Clonal haematopoiesis as a risk factor for therapy-related myeloid neoplasms in patients with chronic lymphocytic leukaemia treated with chemo-(immuno)therapy
Jazyk angličtina Země Anglie, Velká Británie Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
35277855
DOI
10.1111/bjh.18129
Knihovny.cz E-zdroje
- Klíčová slova
- CHIP and FCR, CLL, t-MN,
- MeSH
- chronická lymfatická leukemie * farmakoterapie genetika patologie MeSH
- klonální hematopoéza genetika MeSH
- lidé MeSH
- mutace MeSH
- protokoly antitumorózní kombinované chemoterapie škodlivé účinky MeSH
- rizikové faktory MeSH
- sekundární malignity * etiologie genetika MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Clonal haematopoiesis of indeterminate potential (CHIP) may predispose for the development of therapy-related myeloid neoplasms (t-MN). Using target next-generation sequencing (t-NGS) panels and digital droplet polymerase chain reactions (ddPCR), we studied the myeloid gene mutation profiles of patients with chronic lymphocytic leukaemia (CLL) who developed a t-MN after treatment with chemo-(immuno)therapy. Using NGS, we detected a total of 30 pathogenic/likely pathogenic (P/LP) variants in 10 of 13 patients with a t-MN (77%, median number of variants for patient: 2, range 0-6). The prevalence of CHIP was then backtracked in paired samples taken at CLL diagnosis in eight of these patients. Six of them carried at least one CHIP-variant at the time of t-MN (median: 2, range: 1-5), and the same variants were present in the CLL sample in five cases. CHIP variants were present in 34 of 285 patients from a population-based CLL cohort, which translates into a significantly higher prevalence of CHIP in patients with a CLL who developed a t-MN, compared to the population-based cohort (5/8, 62.5% vs. 34/285, 12%, p = 0.0001). Our data show that CHIP may be considered as a novel parameter affecting treatment algorithms in patients with CLL, and highlight the potential of using chemo-free therapies in CHIP-positive cases.
Clinic for Hematology Clinical Center of Serbia Belgrade Serbia
Department of Biomedicine and Prevention University of Tor Vergata Rome Italy
Department of Clinical Genetics Uppsala University Hospital Uppsala Sweden
Department of Molecular Medicine and Surgery Karolinska Institutet Stockholm Sweden
Department of Translational and Precision Medicine Hematology 'Sapienza' University Rome Italy
Division of Hematology University of Turin Turin Italy
Hematology and Clinical Immunology Department of Hematology Hospital of Padua Padua Italy
Hematology Department and HCT Unit G Papanicolaou Hospital Thessaloniki Greece
Institute of Applied Biosciences Center for Research and Technology Hellas Thessaloniki Greece
UniCamillus Saint Camillus International University of Health Sciences Rome Italy
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Jaiswal S, Fontanillas P, Flannick J, Manning A, Grauman PV, Mar BG, et al. Age-related clonal hematopoiesis associated with adverse outcomes. N Engl J Med. 2014;371(26):2488-98.
Genovese G, Kahler AK, Handsaker RE, et al. Clonal hematopoiesis and blood-cancer risk inferred from blood DNA sequence. N Engl J Med. 2014;371(26):2477-87.
van Zeventer IA, Salzbrunn JB, de Graaf AO, van der Reijden BA, Boezen HM, Vonk JM, et al. Prevalence, predictors, and outcomes of clonal hematopoiesis in individuals aged >/=80 years. Blood Adv. 2021;5(8):2115-22. https://doi.org/10.1182/bloodadvances.2020004062
Young AL, Challen GA, Birmann BM, Druley TE. Clonal haematopoiesis harbouring AML-associated mutations is ubiquitous in healthy adults. Nat Commun. 2016;7:12484.
Jaiswal S, Ebert BL. Clonal hematopoiesis in human aging and disease. Science. 2019;366(6465). https://doi.org/10.1126/science.aan4673
Desai P, Roboz GJ. Clonal hematopoiesis and therapy related MDS/AML. Best Pract Res Clin Haematol. 2019;32(1):13-23.
Fianchi L, Pagano L, Piciocchi A, Candoni A, Gaidano G, Breccia M, et al. Characteristics and outcome of therapy-related myeloid neoplasms: report from the Italian network on secondary leukemias. Am J Hematol. 2015;90(5):E80-5.
Hulegardh E, Nilsson C, Lazarevic V, et al. Characterization and prognostic features of secondary acute myeloid leukemia in a population-based setting: a report from the Swedish acute leukemia registry. Am J Hematol. 2015;90(3):208-14.
Takahashi K, Wang F, Kantarjian H, Doss D, Khanna K, Thompson E, et al. Preleukaemic clonal haemopoiesis and risk of therapy-related myeloid neoplasms: a case-control study. Lancet Oncol. 2017;18(1):100-11.
Gillis NK, Ball M, Zhang Q, Ma Z, Zhao YL, Yoder SJ, et al. Clonal haemopoiesis and therapy-related myeloid malignancies in elderly patients: a proof-of-concept, case-control study. Lancet Oncol. 2017;18(1):112-21.
Fabiani E, Falconi G, Fianchi L, Criscuolo M, Ottone T, Cicconi L, et al. Clonal evolution in therapy-related neoplasms. Oncotarget. 2017;8(7):12031-40.
Voso MT, Falconi G, Fabiani E. What's new in the pathogenesis and treatment of therapy-related myeloid neoplasms. Blood. 2021;138:749-57.
Coombs CC, Zehir A, Devlin SM, Kishtagari A, Syed A, Jonsson P, et al. Therapy-related clonal hematopoiesis in patients with non-hematologic cancers is common and associated with adverse clinical outcomes. Cell Stem Cell. 2017;21(3):374-82 e4.
Arends CM, Galan-Sousa J, Hoyer K, Chan W, Jäger M, Yoshida K, et al. Hematopoietic lineage distribution and evolutionary dynamics of clonal hematopoiesis. Leukemia. 2018;32(9):1908-19.
Wong TN, Ramsingh G, Young AL, Miller CA, Touma W, Welch JS, et al. Role of TP53 mutations in the origin and evolution of therapy-related acute myeloid leukaemia. Nature. 2015;518(7540):552-5.
Wong TN, Miller CA, Jotte MRM, Bagegni N, Baty JD, Schmidt AP, et al. Cellular stressors contribute to the expansion of hematopoietic clones of varying leukemic potential. Nat Commun. 2018;9(1):455.
Burger JA. Treatment of chronic lymphocytic leukemia. N Engl J Med. 2020;383(5):460-73.
Eichhorst B, Robak T, Montserrat E, Ghia P, Niemann CU, Kater AP, et al. Chronic lymphocytic leukaemia: ESMO clinical practice guidelines for diagnosis, treatment and follow-up. Ann Oncol. 2021;32(1):23-33.
Wierda WG, Byrd JC, Abramson JS, Bilgrami SF, Bociek G, Brander D, et al. Chronic lymphocytic leukemia/small lymphocytic lymphoma, version 4.2020, NCCN clinical practice guidelines in oncology. J Natl Compr Canc Netw. 2020;18(2):185-217.
Benjamini O, Jain P, Trinh L, Qiao W, Strom SS, Lerner S, et al. Second cancers in patients with chronic lymphocytic leukemia who received frontline fludarabine, cyclophosphamide and rituximab therapy: distribution and clinical outcomes. Leuk Lymphoma. 2015;56(6):1643-50.
Zhou Y, Tang G, Medeiros LJ, McDonnell TJ, Keating MJ, Wierda WG, et al. Therapy-related myeloid neoplasms following fludarabine, cyclophosphamide, and rituximab (FCR) treatment in patients with chronic lymphocytic leukemia/small lymphocytic lymphoma. Mod Pathol. 2012;25(2):237-45.
Hallek M, Cheson BD, Catovsky D, Caligaris-Cappio F, Dighiero G, Döhner H, et al. iwCLL guidelines for diagnosis, indications for treatment, response assessment, and supportive management of CLL. Blood. 2018;131(25):2745-60.
Jeromin S, Weissmann S, Haferlach C, Dicker F, Bayer K, Grossmann V, et al. SF3B1 mutations correlated to cytogenetics and mutations in NOTCH1, FBXW7, MYD88, XPO1 and TP53 in 1160 untreated CLL patients. Leukemia. 2014;28(1):108-17.
Baliakas P, Hadzidimitriou A, Sutton LA, et al. Recurrent mutations refine prognosis in chronic lymphocytic leukemia. Leukemia. 2015;29(2):329-36.
McNerney ME, Godley LA, Le Beau MM. Therapy-related myeloid neoplasms: when genetics and environment collide. Nat Rev Cancer. 2017;17(9):513-27.
Higgins A, Shah MV. Genetic and genomic landscape of secondary and therapy-related acute myeloid leukemia. Genes (Basel). 2020;11(7):749. https://doi.org/10.3390/genes11070749
Lindsley RC, Mar BG, Mazzola E, Grauman PV, Shareef S, Allen SL, et al. Acute myeloid leukemia ontogeny is defined by distinct somatic mutations. Blood. 2015;125(9):1367-76.
Bolton KL, Ptashkin RN, Gao T, Braunstein L, Devlin SM, Kelly D, et al. Cancer therapy shapes the fitness landscape of clonal hematopoiesis. Nat Genet. 2020;52(11):1219-26.
Jain N, O'Brien S. First-line therapy for young patients with CLL. Hematology Am Soc Hematol Educ Program. 2016;2016(1):146-8.
Chen S, Gao R, Yao C, Kobayashi M, Liu SZ, Yoder MC, et al. Genotoxic stresses promote clonal expansion of hematopoietic stem cells expressing mutant p53. Leukemia. 2018;32(3):850-4.
Kumar V, Ailawadhi S, Bojanini L, Mehta A, Biswas S, Sher T, et al. Trends in the risk of second primary malignancies among survivors of chronic lymphocytic leukemia. Blood Cancer J. 2019;9(10):75.
Smith MR, Neuberg D, Flinn IW, Grever MR, Lazarus HM, Rowe JM, et al. Incidence of therapy-related myeloid neoplasia after initial therapy for chronic lymphocytic leukemia with fludarabine-cyclophosphamide versus fludarabine: long-term follow-up of US intergroup study E2997. Blood. 2011;118(13):3525-7.
Cooper JP, Khajaviyan S, Smith SD, Maloney DG, Shustov AR, Warren EH, et al. Outcomes of patients with therapy-related MDS after chemoimmunotherapy for chronic lymphocytic leukemia compared with patients with De novo MDS: a single-institution experience. Clin Lymphoma Myeloma Leuk. 2019;19(6):390-5.
Awan FT, Al-Sawaf O, Fischer K, Woyach JA. Current perspectives on therapy for chronic lymphocytic leukemia. Am Soc Clin Oncol Educ Book. 2020;40:1-10.
